Many fungal pathogens penetrate plant leaves from a specialized cell called an appressorium. The rice blast pathogen Magnaporthe gnsea can also penetrate synthetic surfaces such as poly (vinyl chloride). Previous experiments have suggested that penetration requires an elevated appressorial turgor pressure. In the present report we have used nonbiodegradable Mylar membranes, exhibiting a range of surface hardness, to test the proposition that penetration is driven by turgor. Reducing appressorial turgor by osmotic stress inhibited penetration of these membranes. The size of the turgor deficit required to inhibit penetration was a function of the surface hardness. Penetration of the hardest membranes was inhibited by small decreases in appressorial turgor, while penetration of the softer membranes was sensitive only to large decreases in turgor. Similarly, penetration of the host surface was inhibited in a manner comparable to penetration of the hardest Mylar membranes. Indirect measurements of turgor, obtained through osmotically induced collapse of appressoria, indicated that the infection apparatus can generate turgor pressures in excess of 8.0 MPa (80 bars). We conclude that penetration of synthetic membranes, and host epidermal cells, is accomplished by application of the physical force derived from appressorial turgor.The mechanism of host surface penetration by plant pathogenic fungi has been debated for nearly a century (1-6). The potential role of extracellular enzymes, to facilitate perforation of the host cuticle or cell wall during fungal invasion, is poorly understood (with one exception) due to the complex and ill-defined chemical nature of plant surfaces (7). On the other hand, an essential role for mechanical force during host surface penetration has been proposed for the rice blast fungus Magnaporthe grisea (Hebert) Barr (8). This pathogen produces unicellular infection structures, called appressoria, which adhere tightly to the host surface and produce slender infection pegs that pierce the underlying cell wall. The cell walls of appressoria contain a dense layer of pentaketidederived melanin whose presence is correlated with a build-up of appressorial turgor pressure (8) and is essential for penetration (8,9). In this study, we have inhibited penetration by exposing appressoria to solutions of high osmotic pressure. This approach was used to reduce the hydrostatic pressure (or turgor) within the infection apparatus and to estimate the magnitude of the turgor involved in penetration. Our results offer unequivocal evidence for an extraordinary mechanical component of the mechanism by which appressoria penetrate hard surfaces, but do not exclude a role in host penetration for some other factor such as extracellular enzymes. MATERIALS AND METHODSOrganism and Growth Conditions. These studies were conducted with strain 042 (see ref. 8) of M. grisea (Hebert) Barr, telomorph of Pyricularia grisea Sacc. (10). The time course of infection-structure development in vitro has been well documented ...

The influence of cyclic loading frequency on the tensile fatigue life of a woven-carbon-fiber/SiC-matrix composite was examined at room temperature. Tension-tension fatigue experiments were conducted under load control, at sinusoidal frequencies of 1, 10, and 50 Hz. Using a stress ratio (um,,,/u,,,,) of 0.1, specimens were subjected to maximum fatigue stresses of 310 to 405 MPa. There were two key findings: (1) the fatigue life and extent of modulus decay were influenced by loading frequency and (2) the postfatigue monotonic tensile strength increased after fatigue loading. For loading frequencies of 1 and 10 Hz, the fatigue limit (defined at 1 X lo6 cycles) was approximately 335 MPa, which is over 80% of the initial monotonic strength of the composite; at 50 Hz, the fatigue limit was below 310 MPa. During 1-and 10-Hz fatigue at a maximum stress of 335 MPa, the modulus exhibited an initially rapid decrease, followed by a partial recovery; at 50 Hz, and the same stress limits, the modulus continually decayed. The residual strength of the composite increased by approximately 20% after 1 X lo6 fatigue cycles at 1 or 10 Hz under a peak stress of 335 MPa. The increase in strength is attributed in part to a decrease in the stress concentrations present near the crossover points of the 0" and 90" fiber bundles.

The effect of lateral cracks on strength controlling contact flaws in brittle materials is examined. Inert strength studies using controlled indentation flaws on a range of ceramic, glass, and single crystal materials reveal significant increases in strength at large contact loads, above the predicted load dependence extrapolated from strength measurements at low indentation loads. The increases are explained by the growth of lateral cracks decohesing the plastic deformation zone associated with the contact from the elastically restraining matrix, thereby reducing the residual stress field driving the strength controlling radial cracks. A strength formulation is developed from indentation fracture mechanics which permits inert strengths to be described over the full range of contact loads. The formulation takes account of the decreased constraint of the plastic deformation zone by lateral crack growth as well as post-contact nonequilibrium growth of the radial cracks. Simple extensions permit the strengths of specimens controlled by impact flaws to be described, as well as those failing under nonequilibrium (fatigue) conditions. The implications for materials evaluation using indentation techniques are discussed and the dangers of unqualified use of strength measurements at large indentation loads pointed out. The work reinforces the conclusion that a full understanding of the residual stress field at dominant contact flaws is necessary to describe the strength of brittle materials.